Session Information

Background/Purpose: Psoriatic arthritis (PsA) is an inflammatory disease affecting the joints and connective tissue and is associated with psoriasis of the skin and nails. In our daily clinical routine, patients often report changes in their disease activity with certain foods, despite the ongoing treatment. Choline metabolism has been recently strongly related to inflammation. Dietary intake of choline, through two circulating metabolites, trimethylamine (TMA), and trimethylamine N-oxide (TMAO), are mechanistically linked to cardiovascular inflammation. The objective of this study was to explore the link between choline metabolites and inflammation in PsA.

Methods: Patients with PsA, diagnosed based on the CASPAR criteria, were recruited from the Rheumatology Outpatient Clinic at the University of California, San Diego. A thorough clinical examination, including joint and skin disease evaluations, was conducted. Patients completed a health assessment questionnaire. DAS28, Clinical Disease Index (CDAI) and Simple Disease Index (SDAI) scores and body surface area (BSA) of psoriasis were calculated. Serum concentration of choline metabolites: choline, TMA, TMAO, and betaine were determined by Mass Spectrometry. Inflammatory biomarkers in serum were determined by ELISA. Statistical analysis included means, standard deviation, t-test and Pearson correlation.

Results: 38 patients (average age 47.45 years, standard deviation [SD] 10.29) were recruited. The mean (SDs) of DAS28PCR was 2.24 (1.29). 27 patients (71.05%) had active skin disease, with an average BSA of 4.73 (SD, 14.5). 23.68% of patients had enthesitis, 5.26% had dactylitis and 47.36% had nail involvement. 65.11% received biological therapy (46.42% of them in association with a synthetic disease modifying drug DMARD), 13.95% received sDMARD in monotherapy and 20.9% received symptomatic treatment. We found that TMAO, a choline metabolite, correlated with parameters of disease activity for both skin (BSA) and joint (DAS28, CDAI, SDAI) (Table 1). Choline, TMA and TMAO also correlated with inflammatory markers (Table 2). TMAO was higher in patients with active joint disease (CDAI>2.8) versus patients in remission (CDAI<2.8; p = 0.01) and in patients with higher severity of skin disease (BSA >5%) versus low severity (BSA <5%; p = 0.03).

Conclusion: In our cohort, choline metabolism was associated with inflammation in PsA patients. Since diet is the main source of choline, modulating choline food intake might help to better control disease activity in these patients. Further studies are needed to explore the mechanistic links between choline and TMAO and inflammation.